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Biology subjects

Hurtado de Mendoza, T.

Publications and source records attributed to Hurtado de Mendoza, T..

2 recordsLinked to original sources

Redirecting cytomegalovirus immunity against pancreas cancer for immunotherapy

Immunotherapy shows limited success in pancreatic cancer, largely due to a low mutational burden and immunosuppressive microenvironment. Here we hypothesized that pre-existing antiviral immunity can be redirected to control pancreatic tumors. Cytomegalovirus (CMV, a {beta}-herpesvirus) was chosen, as the majority of the population is infected and it induces an extremely large/broad memory T cell response. Mice latently infected with murine CMV (MCMV) were orthotopically implanted with pancreatic cancer cells and treated with systemic injections of MCMV T-cell epitopes. The therapy promoted preferential accumulation of MCMV-specific T cells within pancreatic tumors, delaying tumor growth and increasing survival. Immunophenotyping and scRNAseq analyses showed these T cells were highly activated and cytotoxic, leading to increased tumor necrosis and caspase-3 activation. Finally, therapy was enhanced when combined with subtherapeutic doses of gemcitabine chemotherapy. Together, these results show that CMV-specific T cells can be repurposed to combat pancreatic cancer. SignificanceOur studies reveal that CMV-specific viral memory T cells can be re-directed to control a solid tumor normally refractory to immunotherapy via a simple, intravenous injection of T cell peptide epitopes. This mutation agnostic approach has significant potential for the development of "off-the-shelf" therapeutics by stimulating pre-existing antiviral memory and it is widely applicable due to the high prevalence of CMV.

cancer biology↗

Tumor-resident regulatory T cells in pancreatic cancer express the αvβ5 integrin as a targetable activation marker

Pancreatic ductal adenocarcinoma (PDAC) has abundant immunosuppressive regulatory T cells (Tregs), which contribute to a microenvironment resistant to immunotherapy. Here, we report that Tregs in the PDAC tissue, but not those in the spleen, express the v{beta}5 integrin in addition to neuropilin-1 (NRP-1), which makes them susceptible to the iRGD tumor-penetrating peptide, which targets cells positive for v integrin- and NRP-1. As a result, long-term treatment of PDAC mice with iRGD leads to tumor-specific depletion of Tregs and improved efficacy of immune checkpoint blockade. v{beta}5 integrin+ Tregs are induced from both naive CD4+ T cells and natural Tregs upon T cell receptor stimulation, and represent a highly immunosuppressive subpopulation of CCR8+ Tregs. This study identifies the v{beta}5 integrin as a marker for activated tumor-resident Tregs, which can be targeted to achieve tumor-specific Treg depletion and thereby augment anti-tumor immunity for PDAC therapy.

cancer biology↗